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Encyclopedia of
Canine Clinical
Pascale Pibot Vincent Biourge Denise Elliott

Scientific Publishing Head of the Nutritional Director of Scientific

Manager, Royal Canin Research Program, Communications,
Communication Royal Canin Research Royal Canin USA
Group Center

This book is reproduced in the IVIS website with the permission of Royal Canin.
IVIS thanks Royal Canin for their support.
Lisa M.

Cardiovascular diseases:
John E. RUSH
DVM, MS, Dipl
ACVIM (Cardiology),
nutritional modulation

1 - Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
2 - Diagnosis of canine cardiac disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 337
3 - Treatment of cardiac disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 340
4 - Pathophysiology and specific issues of nutritional management . . . . . . . . . . . . . . . . . . . . 341
5 - General issues in feeding dogs with cardiac disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359
Examples of home-prepared diets adapted to the treatment of cardiac complaints . . . . . . . 362
Royal Canin Nutritional Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 364

Cardiovascular diseases:
nutritional modulation

Lisa Freeman graduated from Cummings School of Veterinary Medicine at Tufts University with a Doctorate of Veterinary Medicine in
1991. After completing an internship in Small Animal Medicine and Surgery at North Carolina State University College of Veterinary
Medicine, she completed a residency in Small Animal Clinical Nutrition at the Cummings School of Veterinary Medicine at Tufts
University. She was awarded a PhD in Nutrition by the Tufts University School of Nutrition for her work on cytokines, body composition,
and the effect of fish oil supplementation in canine dilated cardiomyopathy. Lisa Freeman received board certification by the American
College of Veterinary Nutrition in 1997. She is currently an Associate Professor and Clinical Nutritionist at the Cummings School of
Veterinary Medicine at Tufts University. Her research interests include nutritional modulation of cardiac disease and critical care nutrition.

John E. RUSH
DVM, MS, Dipl ACVIM (Cardiology), Dipl ACVECC
John Rush graduated from The Ohio State University School of Veterinary Medicine with a Doctorate of Veterinary Medicine and a Masters
degree in Veterinary Physiology in 1984. After completing an internship in Small Animal Medicine and Surgery at the Animal Medical Center
in New York City, he completed a residency in Small Animal Cardiology and Internal Medicine at the University of Wisconsin-Madison. Dr.
Rush was board certified by the American College of Veterinary Internal Medicine, in the specialty of Cardiology, in 1988. He joined the faculty
at the Cummings School of Veterinary Medicine at Tufts University in 1989, and achieved board certification by the American College of
Veterinary Emergency and Critical Care in 1993. He served as Section Head and residency director for the Emergency and Critical Care Section
until 2003. Dr. Rush is currently a Professor and Associate Chair for the Clinical Sciences Department at the Cummings School of Veterinary
Medicine at Tufts University.

M any scientific advances have improved our knowledge of

cardiac disease and congestive heart failure (CHF) in dogs.
In addition to new cardiac medications, recent advances have
improved our understanding of nutritional interventions and
nutritional pharmacology. Cardiovascular disease is still one of
the most common life-threatening disorders in dogs. Most canine
cardiac diseases cannot be cured and the disease process is
typically progressive, leading to advanced CHF or lethal cardiac
arrhythmias. Nutritional interventions for cardiac disease
remain one of the mainstays of therapy and one of the more
exciting avenues for further scientific investigation.

1 - Epidemiology
1 - Epidemiology
Many risk factors and clinical associations have been identified for cardiovascular disorders in
dogs. Breed predispositions are recognized for most of the common cardiovascular diseases (Table
1). Many small to medium sized dog breeds are predisposed to acquired chronic valvular disease
(CVD; endocardiosis), while dilated cardiomyopathy (DCM) and pericardial disease are the most
common causes of congestive heart failure (CHF) in large breed dogs.

Certain cardiovascular disorders are recognized to have a sex predisposition; for example, female
dogs are predisposed to patent ductus arteriosus and male dogs are predisposed to CVD, idiopa-
thic pericardial disease, and bacterial endocarditis.

Dogs with renal or adrenal disease can develop systemic hypertension and this can predispose or
contribute to existing cardiac disease.

2 - Diagnosis of canine cardiac disease

Congenital and acquired cardiac diseases often lead to similar compensatory responses and neuroen-
docrine activation. Due to the similarities in response of the heart, systemic and pulmonary vascula-
ture and the neuroendocrine systems, several common historical findings and clinical signs result from
most of the canine cardiovascular diseases. FINDINGS IN DOGS WITH
Clinical signs
- Coughing
Common historical complaints include cough, shortness of breath, and syncope (Table 2). Car- - Gagging
diac disease can be quite advanced when the owner is first able to detect clinical abnormality, - Shortness of breath or difficulty
however many cardiac diseases can be detected by the attending veterinarian well in advance of breathing
- Inability to sleep comfortably through
the development of clinical signs.
the night
- Fainting or "seizure" (syncope)
Most congenital cardiac diseases are accompanied by a loud cardiac murmur. The most common - Weight loss
form of cardiovascular disease in the dog, CVD, typically has a cardiac murmur that can be rea- - Abdominal distension
dily identified well before outward clinical signs of cardiovascular disease are evident. The abnor- - Weakness
- Exercise intolerance
malities that are most commonly identified on physical examination from dogs with cardiovas-

- Poor growth (congenital heart disease)
cular disease are listed in Table 3.



Cardiac murmur Dyspnea

Cardiac gallop Pulmonary crackles
Cardiac arrhythmia Ascites
Tachycardia Abdominal organomegaly
Bradycardia Cyanosis
Weak arterial pulses Mucous membrane pallor
Pulsus paradoxus Delayed capillary refill time (> 2 seconds)
Jugular vein distension

2 - Diagnosis of canine cardiac disease


(Compiled from Buchanan, 1992; Kittleson, 1998; Sisson, 2000b; and the computer database
at Cummings School of Veterinary Medicine at Tufts University)

Breed Cardiovascular disease predisposition Breed Cardiovascular disease predisposition

Airedale Terrier PS Keeshond PDA, Tetralogy of Fallot, MVD

Akita Pericardial disease Kerry Blue Terrier PDA

Basset Hound PS Labrador Retriever TVD, PS, PDA, DCM, supraventricular tachycardia,
pericardial disease
Beagle PS, CVD Maltese

Bichon Frisé PDA, CVD Mastiff PS, MVD

Boston Terrier CVD, HBT Miniature Pinscher CVD

Boxer SAS, PS, ASD, Boxer cardiomyopathy, Miniature Schnauzer PS, CVD, sick sinus syndrome
HBT, BE, vasovagal syncope

Boykin Spaniel PS Newfoundland SAS, PS, DCM

Bull Terrier MVD, acquired mitral and aortic fibrosis Old English Sheepdog DCM, atrial standstill

Cavalier King Charles

CVD Papillon CVD

Chihuahua PS, PDA, CVD Pomeranian PDA, sick sinus syndrome, CVD

Chow Chow PS, CTD, VSD Poodle (miniature and toy) PDA, CVD

Cocker Spaniel PDA, PS, CVD, DCM, sick sinus syndrome Portuguese Water Dog Juvenile DCM

Collie PDA Rottweiler SAS, DCM, BE

Dalmatian DCM Saint Bernard DCM

Dachshund CVD Samoyed PS, ASD, SAS, VSD


Doberman Pinscher ASD, DCM Scottish Deerhound DCM

English Bulldog PS, SAS, VSD, MVD, Tetralogy of Fallot Scottish Terrier PS

English Springer Spaniel VSD, PDA, atrial standstill Shetland Sheepdog PDA

Fox Terrier PS, CVD Terrier breeds PS, CVD

German Shepherd PDA, SAS, TVD, MVD, PRAA, juvenile ventricular Weimaraner TVD, peritoneopericardial diaphragmatic hernia
arrhythmia, pericardial disease, DCM, BE
German Short-Haired
Pointer SAS, HCM, pericardial disease, BE Welsh Corgi PDA

Golden Retriever SAS, MVD, TVD, DCM, pericardial disease, BE West Highland White Terrier PS, VSD, sick sinus syndrome, CVD

Great Dane MVD, TVD, SAS, PRAA, DCM Whippet CVD

Irish Setter PRAA, PDA Yorkshire Terrier PDA, CVD

Irish Wolfhound DCM, atrial fibrillation

Key: ASD = Atrial septal defect, BE = Bacterial endocarditis, CTD = Cor triatriatum dexter, CVD = Chronic valvular disease,
DCM = Dilated cardiomyopathy, HBT = Heart base tumor, HCM = Hypertrophic cardiomyopathy, MVD = Mitral valve dysplasia
PDA = Patent ductus arteriosus, PRAA = Persistent right aortic arch, PS = Pulmonic stenosis, SAS = Subaortic stenosis,
TVD = tricuspid valve dysplasia, VSD = ventricular septal defect.

2 - Diagnosis of canine cardiac disease
Diagnostic tests
Once cardiovascular disease is established as a differential dia- FIGURE 1 - ECHOCARDIOGRAPHY INDICATING DILATED
gnosis, a battery of routine tests are often performed to confirm
cardiovascular disease, establish the severity of disease, and
permit an informed decision to be made regarding treatment.

An electrocardiogram should be performed in all dogs with LA

evidence of cardiac arrhythmia, including those with arrhyth-
mia noted on cardiac auscultation and those with femoral
arterial pulse deficits, bradycardia, tachycardia, or a history of
syncope, seizure, or collapse.

Thoracic radiographs are indicated to establish whether CHF

is present and to help determine the degree of cardiac enlar-

© Bussadori
gement, the size of the pulmonary vessels, and the size of the
caudal vena cava. Thoracic radiographs are the best diagnos-
tic test to exclude respiratory diseases as either the cause or a
contributor to the animal’s clinical signs. For many cardiovas- Right parasternal long axis view showing the dilatation of the left atrium
cular diseases, echocardiography is the key diagnostic test to (LA) and left ventricule (LV).
establish the exact cause of the disease. Echocardiography also
facilitates the evaluation of cardiac chamber enlargement and
permits quantitative evaluation of cardiac chamber size, wall
thickness, and myocardial and valve function (Figure 1).
In dogs with congenital disease, echocardiography is used to Dilated cardiomyopathy may be
confirm the type of defect, establish the severity of the defect, associated with taurine deficiency in
certain breeds, such as the Golden
and is an invaluable aid in offering therapeutic and prognos-
Retriever, the Newfoundland and
tic advice. Echocardiography is a key tool for the diagnosis and the Cocker Spaniel.
management of cardiac disease and should be offered in all
cases where serious cardiovascular disease is a differential dia-
Many additional tests are useful in the diagnosis and manage-

© Hermeline

ment of dogs with cardiac disease.

- Heartworm (Dirofilaria immitis) antigen testing should be
carried out in dogs from endemic areas.
- A complete blood count and biochemistry profile should be
carried out to search for concurrent diseases and establish
baseline values prior to therapy. Alterations in blood urea
nitrogen, creatinine, and the serum electrolytes sodium,
potassium, chloride and magnesium can develop following
the initiation of various cardiac medications, and knowled-
ge of these alterations is useful in selecting or altering the diet.
- Plasma and whole blood taurine levels may be indicated in
dogs with evidence of reduced systolic function on echocar-
© Hermeline

© Bouveron

diography, especially in certain breeds of dogs (e.g. Cocker

Spaniel, Golden Retriever, Newfoundland) and in dogs
consuming certain diets (see below).
- Measurement of systemic blood pressure is useful to exclude systemic hypertension as a contri-
buting factor to the cardiovascular disease. In addition, when hypotension develops following
initiation of pharmacologic therapy, a baseline blood pressure measurement can be used for com-
- A variety of additional specialized cardiovascular tests, such as Holter monitor recorders, event
monitor recorders, computed tomography, phonocardiography, and cardiac catheterization are
available for specific clinical settings.
3 - Treatment of cardiac disease

3 - Treatment of cardiac disease

It is beyond the scope of this chapter to mention the appropriate treatment for each cardiovascu-
lar disease recognized in dogs and the reader is referred to the many excellent textbooks on spe-
cific pharmacologic or surgical treatments (Kittleson & Kienle, 1998; Fox et al, 1999; Kittleson,
2000; Sisson et al, 2000a; Ware & Keene, 2000). Common cardiovascular medications include
furosemide, angiotensin converting enzyme (ACE) inhibitors, digoxin, positive inotropes, beta-
blockers, antiarrhythmic drugs, and additional diuretics such as thiazide diuretics and aldostero-
ne receptor blockers (eg, spironolactone). Medications used in an individual patient can impact
appropriate diet selection (see below).

In general, dietary management of dogs with cardiac disease depends upon the clinical signs and
stage of heart failure, rather than the underlying disorder. Therefore, the dietary management of
a dog with CHF secondary to ventricular septal defect or bacterial endocarditis would be similar
to that of a dog with CVD and CHF. When selecting a diet for a dog with cardiac disease, clini-
cians should take into consideration a number of factors including clinical signs and laboratory
parameters. Another important issue to consider is the dog's stage of disease. In the face of acute
CHF, the initial goal should be to titrate medication doses and to get the dog stabilized. In a dog
with pulmonary edema or pleural effusion, the only diet change routinely advised during the ini-
tial period or even when first discharging the dog is to limit intake of very high sodium diets or
high sodium treats. Once the dog is home and stabilized on medications, a gradual change to a
new diet can be made - usually at the time of the first recheck 7-10 days after discharge. Forced
dietary changes when the animal is sick or starting new medications may induce food aversions.

Failure to respond to pharmacologic and nutritional therapies can be the result of advanced or
progressive disease, drug side effects, or incorrect diagnosis. Common pitfalls in the treatment of
dogs with cardiac disease are shown in Table 4.


Older small breed dogs with a Large breed dogs with acquired Failure to accept a new diet Anorexia
cardiac murmur often have cardiac disease often have either Causes can include abrupt change, Both congestive heart failure and
concurrent respiratory disease dilated cardiomyopathy or particularly if the diet is introduced drug side effects can lead to
and it can be difficult to pericardial disease at the same time that drug anorexia. Failure to eat a cardiac
determine whether the clinical Since both of these diseases interventions are being introduced diet is too often attributed to lack
signs result from respiratory can occur without significant or adjusted. of palatability for the diet rather
or cardiac disease abnormalities on cardiac than consideration of the many other
Thoracic radiographs should always auscultation, there may be a delay factors that might impact appetite.
be obtained prior to initiation of in accurate diagnosis unless
diuretics and other cardiac one maintains a high degree of
medications. suspicion for these diseases.

4 - Pathophysiology and specific issues of nutritional management
4 - Pathophysiology and specific
issues of nutritional management
In addition to medications, optimal treatment of dogs with cardiac disease also includes careful
attention to the diet. Although sodium restriction is the nutritional modification most often
thought of for dogs with cardiac disease (and sometimes is the only nutrient modification thought
of), adjustment of a variety of nutrients may be beneficial for these animals. Research is now begin-
ning to show that dietary factors may be able to modulate canine cardiac disease, either by slo-
wing the progression, minimizing the number of medications required, improving quality of life,
or in rare cases, actually curing the disease.
In the past, the goal of nutritional management for animals with cardiac disease was purely symp-
tomatic. This was primarily due to the limited number of medications available for treatment, and
in that situation, severe sodium restriction was beneficial for reducing fluid accumulation in ani-
mals with CHF. Now, with more effective medications available for use in dogs, severe sodium res-
triction is not critical in most dogs. The emphasis in the nutritional management of dogs with
CHF is on providing the optimal number of calories for the individual patient, avoiding nutritio-
nal deficiencies and excesses, and gaining potential beneficial effects from pharmacologic doses of
certain nutrients.

Optimal weight maintenance

Both weight loss and obesity can be problems in animals with cardiac disease, and can adversely
affect the dog’s health.

> Cardiac cachexia

Dogs with CHF commonly demonstrate weight loss, termed cardiac cachexia (Figure 2). This
weight loss in animals with CHF is unlike that seen in a healthy dog that loses weight. In a heal-
thy animal that is receiving insufficient calories to meet requirements (eg, a starving dog, a dog
on a weight reduction diet), fat serves as the primary energy source and this helps to preserve lean
body mass. In a dog with injury or illness, including CHF, amino acids from muscle are the prima-
ry source of energy, resulting in loss of lean body mass.


a: Cardiac cachexia is often viewed as an end-stage situation like b: Cardiac cachexia is actually a process during which lean
the dog shown here with severe dilated cardiomyopathy and body mass is gradually lost. Cachexia can be very subtle initially
congestive heart failure. and may be manifested only by mild muscle loss over the epaxial
and gluteal muscles.

4 - Pathophysiology and specific issues of nutritional management

Therefore, a loss of lean body mass is the hallmark of cachexia. There is a spectrum of severity of
cachexia and the term does not necessarily equate with an emaciated, end-stage patient (Figures
3 & 4). In the early stages, it can be very subtle and may even occur in obese dogs (i.e. a dog may
have excess fat stores but still lose lean body mass). Loss of lean body mass is usually first noted in
the epaxial, gluteal, scapular, or temporal muscles. Cardiac cachexia typically does not occur until
CHF has developed.



Insufficient calories to meet requirements

Mobilization of amino acids from lean body mass

Adaptation to fat utilisation No adaptive response

Preservation of lean body mass Continued loss of lean body mass

= Simple starvation = Cardiac cachexia


There is a dramatic difference between simple starvation, which occurs in a healthy animal and
cachexia, the weight loss seen in animals with cardiac disease. A healthy animal will primarily
lose fat tissue, whereas cachexia is distinguished by a loss of lean body mass.

Cardiac cachexia can occur with any underlying cause of CHF (eg, DCM, CVD, congenital heart
diseases) but most commonly occurs in dogs with DCM, particularly those with right-sided CHF.
In one study of dogs with DCM, over 50% of patients had some degree of cachexia (Freeman et
al, 1998). Loss of lean body mass has deleterious effects on strength, immune function, and sur-
vival, so it is important to recognize cachexia at an early stage to explore opportunities to mana-
ge it effectively (Freeman & Roubenoff, 1994).

The loss of lean body mass in cardiac cachexia is a multifactorial process caused by anorexia,
increased energy requirements, and metabolic alterations (Freeman & Roubenoff, 1994). The ano-
rexia may be secondary to the fatigue or dyspnea or may be due to medication toxicity or feeding
an unpalatable diet. Anorexia is present in 34-75% of dogs with cardiac disease (Mallery et al,
1999; Freeman et al, 2003b). Although not yet measured in dogs with CHF, energy requirements
up to 30% above normal have been documented in people with CHF (Poehlman et al, 1994).

4 - Pathophysiology and specific issues of nutritional management

(a) Despite being trim, this dog has good (b) Early, mild muscle wasting is present (c) Moderate muscle wasting, apparent
muscle tone with no evidence of muscle in this dog, especially in the hindquarters in all muscle groups, is present. Note
wasting (Cachexia score = 0). and lumbar region (Cachexia score = 1). especially the atrophy of the temporal
muscles and muscles over the shoulder
(Cachexia score = 2).

(d) Marked muscle wasting is present in (e) Severe muscle wasting can readily
this dog, as evidenced by the atrophy of all be seen in this dog (Cachexia score= 4).
muscle groups (Cachexia score = 3).

While these factors play a role in the loss of lean body

mass, a major factor in this syndrome is an increased pro- FIGURE 5 - CARDIOVASCULAR AND NUTRITIONAL EFFECTS
duction of inflammatory cytokines, such as tumor necro- (TNF) AND INTERLEUKIN-1 (IL-1)
sis factor (TNF) and interleukin-1 (IL-1) (Freeman et
al, 1998; Meurs et al, 2002). These inflammatory cyto-
kines are known to directly cause anorexia, to increase Hypertrophy
energy requirements, and to increase the catabolism of

lean body mass. Of particular pertinence to cardiac disea-
se, TNF and IL-1 also cause cardiac myocyte hypertro-
phy and fibrosis and have negative inotropic effects Increased energy TNF
IL-1 Negative intropy
(Figure 5). requirements

Nutritional management of dogs with cardiac cachexia

consists primarily of providing adequate calories and protein Loss of lean body Fibrosis
and modulating cytokine production. mass

Anorexia can be detrimental to the dog with CHF in more

than one way. Anorexia can be deleterious because it contri-
butes to the syndrome of cardiac cachexia but, in addition, anorexia is one of the most common fac-
tors that contribute to a dog owner's decision of euthanasia. In one study of owners of dogs euthanized
for CHF, anorexia was one of the most common contributing factors to the euthanasia decision (Mal-
lery et al, 1999). Anorexia is more common in dogs with CHF compared to asymptomatic dogs, and
it also is more common in dogs with DCM compared to dogs with CVD (Freeman et al, 2003b).

One of the most important issues for managing anorexia is to maintain optimal medical control of CHF.
An early sign of worsening CHF is a reduction in food intake in a dog that has previously been eating
well. Another possible cause of decreased appetite is the side effects of medications. Digoxin toxicity
or azotemia secondary to ACE inhibitors or overzealous diuretic use can both cause anorexia. Ensuring
a diet that is palatable to the dog while maintaining other nutritional goals is key to minimizing the

4 - Pathophysiology and specific issues of nutritional management


1. Anorexia is sometimes an early sign

of worsening heart failure and it is
important to assess the patient for 4. Warm the food to room temperature
optimal medical control of heart

5. Feed smaller, more frequent meals

2. Assess the patient for digoxin

toxicity or other medication
6. Add flavor enhancers (yogurt,
maple syrup or cooked meat)

3. Change to a more palatable diet 7. Consider fish oil supplementation

(e.g. canned to dry or dry to
canned, a different brand,
a balanced home-made diet)

effects of cachexia in dogs with CHF. Tips that may assist in food intake include feeding small, more
frequent meals or warming the food to body temperature (or for some dogs, feeding refrigerated food
increases appetite). Gradual introduction of a more palatable diet may be beneficial for some dogs (e.g.,
switching from a dry food to a canned food, changing to a different brand, or having a veterinary nutri-
tionist formulate a balanced homemade diet). It also may be useful to use flavor enhancers to increa-
se food intake (e.g., yogurt, maple syrup, or honey) (Figure 6).

Modulation of cytokine production can also be beneficial for managing cardiac cachexia. Although
specific anti-TNF agents have not proven to be beneficial for people with CHF, dietary supplementa-
tion may be a safer method of reducing inflammatory cytokines. One method of decreasing the pro-
duction and effects of cytokines is with n-3 polyunsaturated fatty acid supplementation (see discussion
of n-3 fatty acids below). Supplementation of fish oil, which is high in n-3 fatty acids, can decrease
cytokine production in dogs with CHF and improve cachexia (Freeman et al, 1998). A reduction of
IL-1 has been correlated with survival in dogs with CHF (Freeman et al, 1998).

Optimal medical and nutritional therapy can help to reverse cachexia and improve nutritional status.
Nutritional status is difficult to measure objectively in the ill patients but one parameter that can be
evaluated is insulin-like growth factor-1 (IGF-1). In people and in dogs, IGF-1 concentrations have
been used as an indicator of nutritional status (Clark et al, 1996; Maxwell et al, 1998). Mean IGF-1
concentrations have been shown to be positively correlated with survival, suggesting that maintaining
good nutritional status may be able to improve survival (Freeman et al, 1998). In people with CHF,
the presence of cachexia has proven to be a poor prognostic indicator (Anker et al, 2003; Davos et al,

> Obesity
Although many dogs, particularly those with more advanced cardiac disease, have weight and
muscle loss, some dogs with cardiac disease are overweight or obese (Figure 7). Although cardiac
implications of obesity have not been well-studied in dogs and coronary artery disease is not a

4 - Pathophysiology and specific issues of nutritional management
major concern in dogs, obesity is thought to be deleterious in dogs with cardiac disease because of
its documented adverse effects on cardiac output, pulmonary function, neurohumoral activation,
blood pressure, and heart rate in people and in experimental animal models (Alexander, 1986).
In any obese dog, underlying endocrine diseases such as hypothyroidism and Cushing's disease
should be ruled out, but most obese animals simply suffer from excess consumption of calories.

Weight reduction programs are a difficult and often frustrating endeavor. For information on obe-
Figure 7 - A dog with chronic
sity and weight reduction programs, see Chapter 1. However, one advantage when a dog has car-
valvular disease complicated by
diac disease is that there is automatically an increased incentive for the owner to commit to a severe obesity. Obesity may exacerbate
weight reduction plan. Although this may not ensure success, it aids in the first step of successful the disease. Owners of obese dogs with
weight loss. cardiac disease often report that, when
the dog loses weight, it acts less dyspneic
As with any weight reduction program, it is critical to perform a careful dietary history to deter- and more active.
mine and control all sources of caloric intake. This diet history is also beneficial in finding other
food sources for the dog that may be contributing both calories and sodium. Typically, the pet food
is only one source of calories for the pet and as many, or more, calories may be consumed from
treats and table food. In one study of dogs with cardiac disease, calorie intake from treats and table
food ranged from 0-100%, with a median calorie intake from treats of 19% (Freeman et al, 2003b).
Therefore, it is important to recommend specific treats that are reduced in both calories and
sodium. Fresh non-starchy vegetables (or frozen/canned forms that are labeled as, “no salt added”)
are excellent low calorie treats for dogs that are obese and have cardiac disease.

If possible, an exercise program will help with the weight reduction program but, for dogs with
CHF in which exercise restriction is recommended, this is not possible. For these dogs, the weight
reduction program must rely on control of calorie intake.

Preventing nutrient excesses

Veterinarians have extrapolated from the human
literature since the 1960's in applying nutritional
recommendations to dogs with cardiac disease. IN HEART DISEASE

> Sodium and chloride

Renal Stimulation of
A prime example is sodium restriction. Healthy dogs perfusion Juxtaglomerular Cells Renin
can easily excrete excess dietary sodium in the urine
but, even before clinical signs become apparent in
dogs with cardiac disease, there is activation of the
renin-angiotensin-aldosterone (RAA) system and Angiotensinogen Angiotensin I
abnormal excretion of sodium (Figure 8) (Barger et Angiotensin
al, 1955). Based on this pathophysiologic change, Angiotensin II Converting Enzyme
sodium restriction has been a mainstay of therapy for
dogs with cardiac disease for nearly 50 years. How-
ever, very few studies have been conducted on die- Vasoconstriction Aldosterone Stimulates Thirst
tary sodium in dogs with cardiac disease. Many ques-
tions remain on the specific intake of sodium recom-
mended for dogs with different stages of disease, at Reabsorption Sodium Reabsorption
what stage sodium restriction should be instituted, and Water Water
and if there are any detrimental effects of sodium res-
Blood Volume Expansion
Net Whole Body Sodium and water

4 - Pathophysiology and specific issues of nutritional management

• Normal dogs
Healthy dogs are relatively tolerant toward the sodium content of their diet.
An early study in 1964 showed no significant changes in extracellular water, sodium, or chloride
in normal dogs fed a low sodium diet (Pensinger, 1964). This study also showed that healthy dogs
were able to maintain sodium and potassium balance on both low and high sodium diets.

Two other studies found that normal dogs fed a low sodium diet had no changes in plasma sodium,
chloride, or extracellular fluid volume compared to those fed a high sodium diet (Hamlin et al,
1964; Morris et al, 1976). In 1994, a study examined the effects of a low sodium diet and furose-
mide in healthy dogs with or without captopril (Roudebush et al, 1994). Although there were no
within-group changes in electrolytes in this study, 3 of 6 dogs became hyperkalemic while recei-
ving a low sodium diet plus furosemide and 2 of 6 became hyperkalemic while receiving a low
sodium diet plus furosemide and captopril (Roudebush et al, 1994). The effects of the low sodium
diet alone were not reported.

In normal dogs, low sodium diets caused an increase in plasma renin activity (PRA) and plasma
aldosterone concentration compared to a high sodium diet, although plasma concentrations of
ACE, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and endothelin-1 (ET-1)
remained unchanged (Pedersen et al, 1994a, Pedersen et al, 1994b). Normal dogs receiving enala-
pril while eating a low-sodium diet, however, had an exaggerated increase in PRA and a larger
decrease in ACE and ANP compared to a dogs eating a high sodium diet (Koch et al, 1994). These
investigators also found an inverse correlation between PRA and sodium content of the diet (Koch
et al, 1994).

• Dogs with CHF

Dogs with CHF respond differently to dietary sodium restriction. Sodium restriction is one
method, along with the use of diuretics and venous vasodilators, to treat excessive increases in
preload in patients with CHF. In the 1960's, when few medications were available for treating
dogs with CHF, dietary sodium restriction was one of the few methods of reducing fluid accumu-
lation. In this situation, severe sodium restriction clearly was beneficial in reducing signs of conges-

In one study, dogs with CHF retained sodium on the high sodium diet but did not retain sodium
on the low sodium diet (Pensinger, 1964). Untreated dogs with mild, asymptomatic mitral valve
insufficiency had a larger increase in PRA and PAC and a lower ACE activity when changed from
a high sodium diet to a low sodium diet (Pedersen, 1996). Sodium intake had no effect on endo-
thelin-1, ANP, and AVP (Pedersen, 1996).

A randomized double-blind, placebo-controlled clinical trial of low sodium diets in dogs with CHF
secondary to either CVD or DCM demonstrated no significant changes in neurohormones bet-
ween a low sodium and moderate sodium diet (Rush et al, 2000). Serum sodium and chloride
concentrations decreased significantly while dogs were eating the low sodium diet (Rush et al,
2000). Measures of cardiac size decreased significantly on the low sodium diet compared to the
moderate sodium diet, especially in dogs with endocardiosis (Rush et al, 2000). The effects of a
low sodium diet on survival were not tested.

The biggest gap in the issue of sodium restriction is for dogs with early cardiac disease [Stage I or
II: Table 5] (International Small Animal Cardiac Health Council (ISACHC), 2001). Based on
the pathogenesis of sodium retention, authors in the 1960's recommended institution of low-
sodium diets for dogs when a heart murmur was first detected, even before clinical signs were pre-
sent (Morris, 1976). Only recently have the benefits and potential problems been questioned. One
of the earliest and major compensatory responses in cardiac disease is activation of the renin-
angiotensin-aldosterone (RAA) system. Sodium restriction can further activate the RAA system
(Pedersen et al, 1994a-1994b; Koch et al, 1994).
4 - Pathophysiology and specific issues of nutritional management
International Small Animal Cardiac Health
Description Dietary sodium recommendations
Council Classification*

1 Asymptomatic 1a Signs of heart disease are present but no signs of Severe sodium restriction is not required.
Heart disease is detectable but patient is not compensation, such as volume or pressure overload Counsel the owner to avoid diets high in sodium
overtly affected and does not demonstrate or ventricular hypertrophy, are evident. (>100 mg/100 kcal) and to avoid treats and table
clinical signs of heart failure. Diagnostic foods that are high in sodium.
findings could include a cardiac murmur,
arrhythmia, or cardiac chamber enlargement
that is detectable by radiography or 1b Signs of heart disease are present in conjunction Sodium content of 50-80 mg/100 kcal in the main
echocardiography. with radiographic or echocardiographic evidence of diet.
compensation, such as volume or pressure overload Also counsel the owner to avoid treats and table
ventricular hypertrophy. foods that are high in sodium.

2 Mild to Moderate Heart Failure Sodium content of 50-80 mg/100 kcal in the main
Clinical signs of heart failure are evident at diet.
rest or with mild exercise and adversely affect Greater sodium restriction (<50 mg/100 kcal) is
quality of life. Typical signs of heart failure recommended if large diuretic doses are necessary to
include exercise intolerance, cough, tachypnea, control clinical signs.
mild respiratory distress (dyspnea), and mild Limiting sodium intake from treats and table foods
to moderate ascites. Hypoperfusion at rest becomes more important.
is generally not present. Counsel owner on appropriate methods for
medication administration.

3 Advanced Heart Failure 3a Home care is possible. Sodium content <50 mg/100 kcal in the main diet.
Clinical signs of advanced congestive heart Limiting sodium intake from treats and table foods is
failure are immediately obvious. These clinical very important.
signs include respiratory distress (dyspnea), Counsel owner on appropriate methods for
marked ascites, profound exercise intolerance, medication administration.
or hypoperfusion at rest.

In the most severe cases, the patient is 3b Hospitalization is mandatory because cardiogenic Stabilization of acute CHF should be the goal. Diet
moribund and suffers from cardiogenic shock. shock, life-threatening pulmonary edema, refractory changes should be avoided until the dog is home and
Death or severe debilitation is likely without ascites, or a large pleural effusion is present. stabilized on medications; a gradual change
therapy. to a new diet can be instituted at that time.

Note that these recommendations assume that the dog is not eating high sodium treats, table foods,
or foods used for medication administration in addition to the main diet. If dogs are eating high
sodium foods in addition to the main diet, the owner should be counselled regarding these foods
or a diet lower in sodium should be selected.

*From: International Small Animal Cardiac Health Council.

Thus, severe sodium restriction in dogs with early cardiac disease could theoretically be detrimen-
tal by early and excessive activation of the RAA system. Studies by Pensinger showed that dogs
with cardiac disease but without CHF were able to maintain sodium and potassium balance on
both low and high sodium diets, similar to normal dogs (Pensinger, 1964) but neurohormone
changes were not measured. While any potential detrimental effects of early institution of severe
dietary sodium restriction have not been shown, it is clear that all drug therapies shown to impro-
ve survival in CHF act by blunting neurohumoral activation. Therefore, severe sodium restriction
(i.e., near the AAFCO minimum of 20 mg/100 kcal) is not currently recommended for dogs with
ISACHC Stage 1 or 2 cardiac disease. Conversely, high dietary sodium intake in early disease is
likely detrimental. Table 5 summarizes the authors’ current recommendations, based on available
literature and clinical experience.

4 - Pathophysiology and specific issues of nutritional management

Most owners are unaware of the sodium content of pet foods and human foods and need very spe-
cific instructions regarding appropriate dog foods, acceptable low salt treats, and methods for admi-
nistering medications (Table 6). Owners also should be counselled on specific foods to avoid such
as baby food, pickled foods, bread, pizza, condiments (e.g., ketchup, soy sauce), lunch meats and
cold cuts (e.g., ham, corned beef, salami, sausages, bacon, hot dogs), most cheeses, processed foods
(e.g., potato mixes, rice mixes, macaroni and cheese), canned vegetables (unless “no salt added”),
and snack foods (e.g., potato chips, packaged popcorn, crackers).

Mildly reduced dietary sodium can be achieved with a therapeutic diet designed for animals with
early cardiac disease or with certain diets designed for use in older dogs. If using a diet designed
for senior dogs, be sure to look at the characteristics of the individual product. There is no legal
definition for a senior diet so the levels of calories, protein, sodium, and other nutrients can vary
dramatically between different companies’ products. Diets designed for animals with renal disease
are not recommended for most cardiac patients because of the protein restriction (unless severe
renal dysfunction is present).


• Switch from pills to a compounded, flavored liquid medication. Be cautious in this approach because the
pharmacokinetics of certain drugs may be altered when compounded

• Teach the owner to pill the animal without using foods. This may be done without any devices
or by using devices designed for this purpose

• Use low sodium foods to insert the pills before administration

- Fresh fruit (e.g., banana, orange, melon)
- Low sodium canned pet food
- Peanut butter (labeled as “no salt added”)
- Home-cooked meat (without salt) - not lunch meats

As CHF becomes more severe, more sodium restriction may allow lower dosages of diuretics to be

used to control clinical signs. To achieve severe sodium restriction, it is usually necessary to feed
a commercial therapeutic diet designed for cardiac patients. Typically, these diets are severely res-
tricted in both sodium and chloride; levels of other nutrients vary with the individual product.

Dietary chloride levels are often ignored but research suggests that chloride may be important in
the optimal management of CHF. Research in people has shown that sodium and chloride admi-
nistration are necessary for the full expression of hypertension in people (Boegehold & Kotchen,
1989). Chloride administration also appears to decrease plasma renin activity in salt depleted rats
(Kotchen et al, 1980; Muller, 1986).

The patient with heart failure has chronic activation of the RAA system, which could be signi-
ficantly influenced by dietary chloride. In addition, furosemide is known to block chloride trans-
port in the ascending loop of Henle, and hypochloremia (and hyponatremia) can develop in
advanced CHF. Therefore, chloride is likely to play an important role in the CHF patient. Unfor-
tunately, little is known about optimal dietary intake for CHF patients and additional research
will be required to make specific recommendations.

> Potassium
In the past, when digoxin and diuretics were the mainstays of therapy for people and dogs with
CHF, hypokalemic was a major consideration. Now, ACE inhibitor therapy has gained widespread

4 - Pathophysiology and specific issues of nutritional management
use in the management of dogs with CHF and this medication results in renal potassium sparing.
Therefore, ACE inhibitors are known to cause increased serum potassium, with some animals
developing hyperkalemia (Roudebush et al, 1994; COVE Study Group, 1995; Rush et al, 1998).
This can especially be a problem in animals eating commercial cardiac diets since some commer-
cial cardiac diets contain increased potassium concentrations to counteract the theoretical loss
due to diuretics.

In addition to the importance of the diets' compatibility with current ACE inhibitor use, other
newer cardiac medications may also be used more commonly. Spironolactone, an aldosterone
antagonist and a potassium-sparing diuretic is being used with greater frequency in veterinary
patient after reports of improved survival in human CHF patients (Pitt et al, 1999). This medica-
tion is even more likely than other diuretics to cause hyperkalemia. Finally, many people know
about the association between diuretics and hypokalemia either from their own medical condi-
tion or that of a friend or relative, and some mistakenly give their dogs with CHF bananas or
potassium supplements in an effort to prevent this problem. Routine monitoring of serum potas-
sium is recommended for all patients with CHF, particularly those receiving an ACE inhibitor or
spironolactone. If hyperkalemia is present, a diet with a lower potassium content should be selec-

Preventing nutritional deficiencies

versus nutritional pharmacology
Historically, a variety of nutritional deficiencies have been known to cause cardiac disease in various
species. These include thiamine, magnesium, vitamin E, selenium, and taurine. Although nutritional
deficiencies are generally uncommon (except in owners feeding unbalanced homemade diets), they
may still play a role in some cardiac diseases of dogs. Nutritional deficiencies may also develop secon-
dary to the disease or its treatment. There is also blurring of the lines between the benefits of correc-
ting a nutritional deficiency (e.g. as in a cat with taurine deficiency-induced dilated cardiomyopathy)
and the pharmacological effects of a nutrient (e.g. the positive inotropic effects of taurine). In addi-
tion, new information is coming out on species and even breed differences in nutrient requirements.
Thus, there appears to be much more to providing optimal levels of nutrients than just preventing a

> Protein and amino acids

• Protein
In addition to sodium restriction, the dietary recommendations in the 1960's for dogs with CHF
were to restrict protein intake to “reduce the metabolic load on congested, aging, and diseased
kidneys and liver” (Pensinger, 1964). Restricting protein can actually be detrimental in terms of
lean body mass loss and malnutrition. Dogs with CHF should not be protein restricted, unless they
have concurrent advanced renal disease. Some of the diets designed for dogs with cardiac disease
are low in protein (3.6-4.2 gm/100 kcal). In addition, some veterinarians recommend protein-res-
tricted renal diets for dogs with cardiac disease because these diets often (but not always) are also
moderately sodium restricted.

Unless severe renal dysfunction is present (i.e., serum creatinine>3.0 mg/dL), high-quality pro-
tein should be fed to meet canine AAFCO minimums for adult maintenance requirements
(5.1 gm/100 kcal; Association of American Feed Control Officials (AAFCO), 2005). In one study,
daily protein intake of dogs with cardiac disease ranged from 2.3-18.8 g/100 kcal so some dogs with
cardiac disease are clearly not eating sufficient dietary protein (Freeman et al, 2003b).

Another misconception that impacts cardiac disease is the still widespread belief that dietary pro-
tein should be restricted in early renal disease (see chapter 8). Although the majority of dogs trea-
ted with ACE inhibitors do not develop azotemia, some dogs receiving ACE inhibitors can deve-
lop azotemia (COVE Study Group, 1995). Azotemia occurs more frequently when ACE inhibi-

4 - Pathophysiology and specific issues of nutritional management

tors are used in conjunction with diuretics although, in a small number of dogs, azotemia can deve-
lop from ACE inhibitors alone. When concurrent ACE inhibitor and diuretic use causes azote-
mia, reduction of the furosemide dose is indicated to reduce azotemia. A protein-restricted diet is
not necessary in this situation unless medication changes do not correct the problem and the renal
disease progresses.

• Taurine
The association between taurine and feline DCM described in the late 1980’s prompted investi-
gators to examine the role of taurine in canine DCM (Pion et al, 1987). Unlike cats, dogs are
thought to be able to synthesize adequate amounts of taurine endogenously and taurine is not
considered to be required in canine diets. Although initial studies showed that most dogs with
DCM did not have low plasma taurine concentrations, certain breeds of dogs with DCM (eg, Coc-
ker Spaniels and Golden Retrievers) did have low taurine concentrations (Kramer et al, 1995).
The association between dogs with DCM and low taurine concentrations has been best establi-
shed in the American Cocker Spaniel (Kramer et al, 1995; Kittleson et al, 1997).

In a study by Backus et al, 12 of 19 Newfoundlands tested had taurine concentrations consistent

with taurine deficiency. However, none of these dogs had DCM (Backus et al, 2003). Other com-
monly reported breeds of dogs with DCM and taurine deficiency include Golden Retriever, Labra-
dor Retriever, Saint Bernard, English Setter (Freeman et al, 2001; Fascetti et al, 2003).
When concurrent ACE inhibitor
and diuretic use causes azotemia,
The first question about the relationship between canine DCM and taurine deficiency is whether
reduction of the diuretic dose is
indicated to reduce azotemia. DCM is caused by dietary deficiency.
A protein restricted diet is not
necessary in this situation unless In one retrospective study, 20 of 37 dogs with DCM tested for plasma and whole blood taurine
medication changes do not correct concentrations were considered to be taurine-deficient (Freeman et al, 2001). There was no signi-
the problem and the renal disease
ficant difference in mean dietary taurine content (based on manufacturers’ information) between
taurine deficient and non taurine deficient dogs, nor was there a correlation between dietary
content and circulating taurine concentrations (Freeman et al, 2001). Of the taurine deficient
dogs, 7 were eating a lamb and rice based diet and seven were eating an increased fiber diet.

Twelve dogs with DCM and taurine deficiency were reported to be eating dry diets containing

lamb meal, rice, or both as primary ingredients (Fascetti et al, 2003).

In another study, 131 normal dogs were tested for plasma and whole blood taurine concentrations.
In this study, dogs consuming diets containing rice bran or whole grain rice had lower taurine
concentrations (Delaney et al, 2003). Thus, it may be the rice bran component of diets that affects
taurine concentrations although lamb meal also is known to have decreased amino acid digesti-
bility (Johnson et al, 1998).

Alternatively, dietary protein quality and quantity may also play a role in taurine deficiency. In
one study, a group of Beagles fed a low taurine, very low protein diet for 48 months had a decrea-
se in whole blood taurine concentrations and 1 of the 16 dogs developed DCM (Sanderson, 2001).

Finally, some dog breeds may be predisposed to taurine deficiency when fed certain types of diets
because of higher requirements or breed-specific metabolic abnormalities.
© Psaila

A second question that still remains is whether taurine supplementation reverses DCM in dogs
In a retrospective study, of the taurine with concurrent taurine deficiency.
deficient dogs, 7 were eating a lamb
and rice based diet and 7 were eating In one small study, 11 Cocker Spaniels supplemented with taurine and carnitine showed impro-
an increased fiber diet.
vement in clinical parameters and echocardiographic measurements (Kittleson et al, 1997). Whe-
ther the response would be similar with taurine alone remains to be seen. In one small retrospec-

4 - Pathophysiology and specific issues of nutritional management
tive study that compared dogs with DCM that were taurine deficient and were treated with tau-
rine (plus medical therapy) to dogs that were not taurine deficient, there was no difference in the
number that were able to discontinue medications, in the furosemide dosage, in echocardiogra- Minimum taurine requirements for
phic measurements, or survival (Freeman et al, 2001). Another retrospective study of 12 dogs with dogs have not been established by
AAFCO, but the minimum taurine
DCM and taurine deficiency showed a within-group improvement in E-point to septal separation requirement for adult cats is
and fractional shortening after taurine supplementation but there was no comparison group (Fas- 25 mg/100 kcal for dry food and
cetti et al, 2003). 50 mg/100 kcal for canned foods
(AAFCO, 2005). A diet with a
Response to therapy may be breed dependent. In a study of a litter of Portugese Water Dogs with taurine content of 50 mg/100 kcal
would provide approximately
DCM, taurine was below the reference range in eight of eight puppies tested, and DCM was dia- 1000 mg/day of taurine to a 40 kg
gnosed in eight of the nine puppies (Alroy, 2000). Taurine supplementation was instituted in 6 of dog.
the puppies, which significantly increased plasma and whole blood taurine concentrations as well
as cardiac function (Alroy, 2000). In a study of Beagles fed a low taurine, very low protein diet for
48 months, the one dog that developed DCM had improvement in
fractional shortening after three months of taurine supplementation
(Sanderson et al, 2001). Some of the potential benefits of taurine in
dogs with DCM may be due to its positive inotropic effects or role in
calcium regulation in the myocardium. Beneficial effects of taurine
have been shown in animal models with experimentally-induced
heart failure and in unblinded human clinical trials (Elizarova et al,
1993, Azuma, 1994).

While it is unlikely that the breeds at high risk for DCM such as the
Doberman Pinscher or the Boxer have taurine deficiency, certain
breeds (eg, Cocker Spaniel, Newfoundlands, Golden Retrievers) and
atypical breeds (eg, Scottish Terrier, Border Collie) may have concur-
rent taurine deficiency. Therefore, in these latter breeds, measuring
plasma and whole blood taurine concentrations is recommended. In

© Renner
addition, taurine concentrations should be measured in dogs with
DCM that are eating lamb meal and rice, very low protein, or increa-
In Cocker Spaniels with DCM,
sed fiber diets. Although the extent of the benefit of supplementation measuring plasma and whole blood
is not yet clear, taurine supplementation is recommended until plasma and whole blood taurine taurine concentrations is
concentrations from the patient are available. Even in dogs with taurine deficiency that do recommended.

respond to taurine supplementation, the response is generally not as dramatic as in taurine defi-
cient cats with DCM. The optimal dose of taurine for correcting a deficiency has not been deter-
mined but the currently recommended dose is 500-1000 mg q 8-12 hours. Taurine can be provi-
ded as a supplement although certain diets may contain enough taurine to raise plasma taurine

• Arginine
Nitric oxide is an endogenous vascular smooth muscle relaxant. It is synthesized from L-arginine
and molecular oxygen (Figure 9).

Circulating nitric oxide is elevated in people with CHF, regardless of the underlying cause and in
two studies of dogs and cats with heart disease (De Belder et al, 1993; Comini et al, 1999; De Lafor-
cade et al, 2000; Freeman et al, 2003a). However, one study of dogs showed lower nitric oxide
concentrations in dogs with untreated CVD (Pedersen et al, 2003). High circulating nitric oxide
levels may have an initial beneficial compensatory effect but can be detrimental when this res-
ponse is prolonged. High levels of nitric oxide can have a negative inotropic effect and can decrea-
se the responsiveness to beta-adrenergic stimulation (Gulick et al, 1989; Yamamoto et al, 1997).
There appear to be competing responses occurring in CHF. While iNOS is upregulated in patients
with CHF producing high circulating levels of nitric oxide, eNOS is actually downregulated and
reduces endothelium-dependent vasodilation (Agnoletti et al, 1999, Katz et al, 2000).

4 - Pathophysiology and specific issues of nutritional management

The reduction in eNOS and resulting loss of normal vasodilation have adverse effects in the
patient with CHF (Feng et al, 1998). People with CHF have a reduction of peripheral blood flow
both at rest and during exercise (Maguire et al, 1998). This abnormality may contribute to exer-
cise intolerance in these patients. Endothelial dysfunction has also been demonstrated in dogs
with experimentally-induced CHF and is associated with decreased gene expression of eNOS
(Wang et al, 1997).

Based on the findings of endothelial dysfunction in patients with CHF, investigators have begun
to study the effects of arginine supplementation in this group. In normal patients, L-arginine sup-
plementation is unlikely to have an effect on nitric oxide production because L-arginine is found
in concentrations much higher than the Km values for NOS (Tsikas et al, 2000). But the situa-
tion in patients with CHF may be very different and, in fact, L-arginine supplementation has been
shown to improve endothelial dysfunction (Kubota et al a, 1997; Feng et al, 1999; Kanaya et al,
1999; Hambrecht et al, 2000). L-arginine supplementation has been tested in people with CHF in
a number of studies (Kubota et al, 1997; Kanaya et al, 1999; Banning & Prendergast, 1999; Bocchi
et al, 2000; Hambrecht et al, 2000). These studies have shown increased circulating concentra-
tions of nitric oxide but improved endothelium-dependent vasodilation and cardiac output. These
studies also have shown reduced heart rate and systemic vascular resistance, with no negative
effects on cardiac contractility or other echocardiographic variables (Kubota et al, 1997; Ham-
brecht et al, 2000; Bocchi et al, 2000). Although one study of arginine supplementation found no
effect on exercise tolerance, another study showed that L-arginine reduced dyspnea in response
to increasing CO2 production during exercise in people with severe chronic heart failure (Kanaya
et al, 1999; Banning & Prendergast, 1999). Thus, while much research is needed in this area, argi-
nine supplementation may provide beneficial effects in patients with CHF.

> Fat
Fat is a source of calories and essential fatty acids and increases
FIGURE 9 - ORIGIN OF NITRIC OXIDE the palatability of the diet. However, depending upon the type of
fat, it can have significant effects on immune function, the pro-
duction of inflammatory mediators and even hemodynamics.

+ + • n-3 fatty acids


Most human and canine diets contain primarily n-6 fatty acids.
nitric oxide synthase (NOS) In n-6 fatty acids (eg linoleic acid, γ-linolenic acid, and arachi-
donic acid), the first double-bond is at the position of the 6th car-
bon from the methyl end. However, n-3 fatty acids [α-linolenic
L-arginine + O2 NO +L-citrulline acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid
(DHA)] have the first double-bond at the 3rd carbon from the
Oxygen Carbon methyl end. Although this seems like a minor change, it confers
Nitrogen Hydrogen very different structure and characteristics to the fatty acid. Plas-
ma membranes normally contain very low concentrations of n-3
fatty acids, but levels can be increased by a food or supplement
enriched in n-3 fatty acids.
The reaction is catalyzed by the enzyme, nitric oxide
synthase (NOS). There are three forms of NOS:
Dogs with heart failure have lower plasma concentrations of eico-
• endothelial NOS (eNOS): eNOS is required for maintenance sapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid
of normal vascular tone and as a physiologic messenger (DHA; 22:6n-6), regardless of the underlying disease (Figure 10)
• neuronal NOS (nNOS): eNOS and nNOS are constitutive (Freeman et al, 1998; Rush et al, 2000). This alteration in plasma
forms and are always produced in low levels fatty acids has also been found in people with various diseases as
• inducible NOS (iNOS): iNOS is inducible by a variety of
inflammatory mediators including the cytokines, tumor necrosis
well, suggesting that metabolic changes may occur in certain
factor (TNF), and interleukin-1 (IL-1), and free radicals. diseases that increase the use of n-3 fatty acids. Therefore, supple-
mentation may improve an absolute or relative n-3 fatty acid

4 - Pathophysiology and specific issues of nutritional management
n-3 fatty acid supplementation also reduces the more inflam- FIGURE 10 - PLASMA FATTY ACID CONCENTRATIONS
matory eicosanoids. n-3 fatty acids are known to reduce the pro- IN DOGS WITH DILATED CARDIOMYOPATHY
duction of the more inflammatory 2- and 4-series eicosanoids TO HEALTHY CONTROL DOGS (N=5)
(eg, there is a shift from production of prostaglandin E2 to pros- (From Freeman et al, 1998)
taglandin E3). In a study of dogs with DCM, dogs supplemen-
ted with fish oil had a greater reduction in prostaglandin E2
production compared to dogs receiving the placebo (Freeman
et al, 1998). This may have benefits in terms of reduced inflam- 3.0
mation. n-3 fatty acids also are known to decrease the produc- 2.8
tion of the inflammatory cytokines, TNF and IL-1, which are 2.4
elevated in CHF (Endres et al, 1989; Meydani et al, 1991; Free- 2.2
man et al, 1998). 2.0

Concentration (%)
Fish oil supplementation reduced cachexia and, in some, but 1.6
not all dogs with CHF-induced anorexia, improved food intake *
(Freeman et al, 1998). Finally, n-3 fatty acids have been shown 1.0
in a number of rodent, primate, and canine models to reduce 0.8
arrhythmogenesis (Charnock, 1994; Kang & Leaf, 1996; Bill- 0.6
man et al, 1999). Many dogs with CVD and most dogs with 0.4 *
DCM have arrhythmias. In some dogs with cardiac disease, sud-
den death due to arrhythmias is the first manifestation of the EPA DHA
disease in otherwise asymptomatic dogs. Therefore, n-3 fatty
acid supplementation may be beneficial even before CHF deve-

• n-3 fatty acid supplementation Dogs with DCM and heart failure had significantly lower plasma
There is controversy as to whether dose of n-3 fatty acids or the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)
concentrations compared to healthy control dogs.
ratio of n-6: n-3 fatty acids is more important for the beneficial *P<0.05.
effects of n-3 fatty acids. Some evidence points to the primary (mean +/- standard deviation)
importance of the total n-3 dose but it may also be important
to avoid a high n-6:n-3 ratio as well. Although an optimal dose

has not been determined, the authors currently recommend a
dosage of 40 mg/kg EPA and 25 mg/kg DHA for dogs with anorexia or cachexia. Unless the diet
is one of a few specially designed therapeutic diets, supplementation will be necessary since other
commercial diets will not achieve this n-3 fatty acid dose. Although an optimal dose has not
been determined, the authors currently
The exact content of EPA and DHA in individual fish oil supplements varies widely. The most recommend a dosage of 40 mg/kg EPA
and 25 mg/kg DHA for dogs with
common formulation of fish oil, however, is one gram capsules that contain 180 mg EPA and
anorexia or cachexia. Unless the diet
120 mg DHA. At this concentration, fish oil can be administered at a dose of 1 capsule per 10 is one of a few specially designed
pounds of body weight to achieve the authors’ recommended EPA and DHA dose. Fish oil with therapeutic diets, supplementation
higher concentrations of EPA and DHA can be obtained from medical supply catalogs and may will be necessary since other
be more feasible for large dogs. commercial diets will not achieve
this n-3 fatty acid dose.

Fish oil supplements should always contain vitamin E as an antioxidant, but other nutrients should
not be included to avoid toxicities. Similarly, cod liver oil should not be used because of the pos-
sibility for vitamins A and D toxicity. Finally, although flax seed oil contains high levels of α-lino-
lenic acid, this fatty acid must be converted to EPA and DHA for its beneficial effects. Species
vary in the ability to make this conversion: dogs have the enzymes to convert it but with limited
efficiency. Therefore, flax seed oil is not recommended as an n-3 fatty acid supplement.

4 - Pathophysiology and specific issues of nutritional management

> Minerals and vitamins

• Potassium
Potassium is an important electrolyte in cardiac patients for a number of reasons. Hypokalemia
potentiates arrhythmias, causes muscle weakness, and predisposes patients to digitalis toxicity. In
addition, Class I antiarrhythmic drugs, such as procainamide and quinidine, are relatively ineffec-
tive in the face of hypokalemia. Hypokalemia was considered to be a common problem in the past
when diuretics were the mainstays of therapy. Many of the medications used in dogs with CHF
can predispose a patient to hypokalemia, including loop diuretics (eg, furosemide) and thiazide
diuretics (eg, hydrochlorothiazide). However, with the increased use of ACE inhibitors, hypoka-
lemia is no longer very common in dogs with CHF.

In addition to medication effects, inadequate dietary intake could predispose a dog to hypokale-
mia. In one study, 49% of dogs with cardiac disease ate less potassium than the AAFCO mini-
mum value (170 mg/100 kcal). Intakes ranged from 37-443 mg/100 kcal (Freeman et al, 2003b).
This suggests that, based on dietary intake alone, some dogs may be predisposed to hypokalemia
(in addition to the risk for hyperkalemia previously discussed) and underscores the importance of
monitoring serum potassium in dogs with CHF.

• Magnesium
Magnesium is an essential prosthetic group in hundreds of enzymatic reactions involving carbo-
hydrate and fatty acid metabolism, protein and nucleic acid synthesis, the adenylate cyclase sys-
tem, and cardiac and smooth muscle contractility. Thus, magnesium plays an important role in
normal cardiovascular function. It is also clear that alterations in magnesium homeostasis in
people and dogs are common, and can have deleterious effects in a variety of cardiovascular condi-
tions including hypertension, coronary artery disease, congestive heart failure, and cardiac
arrhythmias (Resnick, 1984; Rayssiguer, 1984; Gottleib et al, 1990; Iseri, 1986; Cobb & Michell,
1992). In addition, numerous drugs used to treat cardiac conditions, including digoxin and loop
diuretics are associated with magnesium depletion (Quamme & Dirks, 1994). Therefore, dogs with
heart failure receiving these medications have the potential to develop hypomagnesemia. Hypo-
magnesemia can increase the risk of arrhythmias, decrease cardiac contractility, and can poten-
tiate the adverse effects of cardiac medications.

There have been conflicting reports on the prevalence of hypomagnesemia in dogs with cardiac
disease. Reports range from “uncommon” (O'Keefe et al, 1993) to 2/84 (Edwards et al, 1991); fifty
percent (Rush, 2000) to two-thirds of Lasix-treated dogs (Cobb & Michell, 1992).

One of the difficulties in diagnosing magnesium deficiency is that only one percent of the total
Hypokalemia was considered to be body magnesium is in the extracellular space. Therefore, normal serum magnesium does not neces-
a common problem in the past when sarily mean there are adequate total body stores. Serial measurements of serum magnesium are cur-
diuretics were the mainstays of
rently recommended, especially in dogs with arrhythmias or those receiving large doses of diure-
therapy. Many of the medications
used in dogs with CHF can tics. If low serum magnesium concentrations do arise and the dog is eating a diet that is low in
predispose a patient to hypokalemia, magnesium, a diet higher in magnesium may be beneficial. Magnesium concentrations vary wide-
including loop diuretics (eg, ly in commercial pet foods. Commercial reduced sodium diets for dogs can contain between 9-
furosemide) and thiazide diuretics 40 mg magnesium/100 kcal (compared to an AAFCO minimum of 10 mg/100 kcal). If the dog
(eg, hydrochlorothiazide). However,
remains hypomagnesemic, oral magnesium supplementation will be required (e.g. magnesium
with the increased use of ACE
inhibitors, hypokalemia is no longer oxide).
very common in dogs with CHF.
• B vitamins
(Table 7)
Little research has been conducted on the prevalence of B vitamin deficiencies in dogs with car-
diac disease. However, there have long been concerns over the risk of B vitamin deficiencies in
CHF due to anorexia and urinary loss of water soluble vitamins secondary to diuretic use. This

4 - Pathophysiology and specific issues of nutritional management
may be less of a problem now that there are more effective medications for treatment of CHF but
even in one study from 1991, 91% of people with CHF had low thiamine concentrations (Selig-
mann et al, 1991). In this study, patients were being treated with furosemide, ACE inhibitors,
nitrates, and digoxin (where appropriate).
Low doses of furosemide were shown to cause increased urinary loss of thiamine in healthy people
and in rats (Rieck et al, 1999; Lubetsky et al, 1999). Although B vitamin status has not been repor-
ted for dogs with CHF, they may have higher dietary B vitamin requirements. Most commercial
cardiac diets contain increased levels of water soluble vitamins to offset urinary losses so supple-
mentation usually is not required.

> Other nutrients

• Antioxidants
Much attention has been given to antioxidants for their potential role in the prevention and treat-
ment of human cardiac diseases. Reactive oxygen species are a by-product of oxygen metabolism
for which the body normally compensates through the production of endogenous antioxidants.
An imbalance between oxidant production and antioxidant protection (eg, oxidative stress),
however, could increase the risk for cardiac disease (Figure 11). Antioxidants are produced endo-
genously but also can be supplied exogenously. The major antioxidants include enzymatic antioxi-
dants (e.g., superoxide dismutase, catalase, glutathione peroxidase) and oxidant quenchers (e.g.,
vitamin C, vitamin E, glutathione, and β-carotene).
Oxidative stress has been implicated in the development of a number of cardiac diseases. Increa-
sed oxidative stress has been demonstrated in people with CHF (Belch et al, 1991; Keith et al,
1998). In dogs with heart failure, regardless of the underlying cause, there are increased levels of
biomarkers of oxidative stress and a reduction in certain antioxidants, particularly vitamin E (Free-
man et al, 1999; Freeman et al, 2005). These alterations suggest an imbalance between oxidant
stress and antioxidant protection in dogs with CHF.

Additional research is required to evaluate the effect, but antioxidant supplementation may hold
promise in the future for the therapy of animals with cardiac disease.

Name Abbreviations
Thiamin B1
Riboflavin B2
Pantothenic acid (B5*)
Pyridoxine B6
Biotin (B8*)
Folic acid (B9*)
Cobalamin B12
Niacin PP
* also called

• L-Carnitine
L-Carnitine is a quaternary amine (Figure 12) whose major role is in long-chain fatty acid meta-
bolism and energy production. Carnitine deficiency syndromes in people have been associated
with primary myocardial disease and, based on this and its high concentrations in cardiac muscle,
its role in canine DCM also has been of interest.

4 - Pathophysiology and specific issues of nutritional management

L-carnitine deficiency was reported in a family of Boxers in 1991 (Keene et al, 1991). Since that
time, L-carnitine supplementation has been used in some dogs with DCM but no blinded prospec-
tive studies have been done so a causative role has not been established. In human DCM patients,
most studies of L-carnitine have not been well-controlled. However, one randomized, double-blind,
placebo-controlled study showed improved three-year survival in human DCM patients receiving
2 gm/day L-carnitine (Rizos, 2000).

One of the difficult aspects of studying L-carnitine in DCM is that one must measure myocardial
concentrations since plasma concentrations are often normal even in the face of myocardial defi-
ciency. Therefore, the advancement of knowledge of the role of this nutrient in DCM has been
slow. It is not yet clear whether the carnitine
deficiency seen in some dogs with DCM is
FIGURE 11 - ORIGIN OF OXIDATIVE STRESS the cause of the disease or merely secondary
to the development of CHF. One study of
dogs with heart failure induced by rapid
pacing showed that myocardial concentra-
tions decreased in normal dogs after the onset
of CHF (Pierpont et al, 1993). However, even
if L-carnitine deficiency is not the inciting
cause of DCM, supplementation may still
provide benefits by improving myocardial
energy production.
Antioxidants from endogenous
and exogenous origins: L-carnitine supplementation has few side
• Enzymes (superoxide effects but it is expensive and this may be a
Reactive oxygen species
dismutase, catalase, significant deterrent for some owners. The
glutathione peroxidase) authors offer the option of L-carnitine sup-
• Oxidation quenchers
plementation to owners of dogs with DCM,
(vitamin C, vitamin E,
glutathione and β-carotene) especially Boxers and Cocker spaniels, but do
not consider it essential. The minimum or
Oxidative stress comes from the imbalance between optimal dose of L-carnitine necessary to
the production of free radicals and antioxidant replete a dog with low myocardial carnitine
defenses. concentrations is not known, but the cur-

rently recommended dose is 50-100 mg/kg

PO q 8 hours.

• Coenzyme Q10
Coenzyme Q10 is a cofactor required for energy production and has antioxidant properties. There
are a number of mechanisms by which coenzyme Q10 might play a role in cardiac disease. Some
investigators have proposed coenzyme Q10 deficiency as a possible cause for DCM but this has
not been proven. Even in dogs with experimentally-induced CHF, serum coenzyme Q10 levels
were not reduced (Harker-Murray et al, 2000).

The most enthusiasm for coenzyme Q10 has been as a dietary supplement in the treatment of
people or dogs with DCM. Coenzyme Q10 supplementation has anecdotally been reported to be
The minimum or optimal dose beneficial but most of the human studies of coenzyme Q10 supplementation have not been well-
of L-carnitine necessary to replete controlled and results are conflicting. However, some encouraging results have been found (Lang-
a dog with low myocardial carnitine sjoen et al, 1994; Sacher et al, 1997; Munkholm et al, 1999). In one study of dogs with experimen-
concentrations is not known,
but the currently recommended tally-induced CHF, coenzyme Q10 supplementation increased serum, but not myocardial, concen-
dose is 50-100 mg/kg PO q 8 hours. trations (Harker-Murray et al, 2000). The bioavailability of coenzyme Q10 varies in different tis-
sues and also depends upon the degree of tissue deficiency in that tissue.

The current recommended dose in canine patients is 30 mg PO BID, although up to 90 mg PO

BID has been recommended for large dogs. The purported benefits of supplementation include
5 - General issues in feeding dogs with cardiac disease

Discovered in 1905, L-carnitine is synthetized

in dogs from lysine and methionine, if vitamin C
and pyridoxine (vit B6) are present. It is a
quaternary amine that acts as a water soluble
vitamin. Carnitine can be synthetized in D
or L forms, but L-carnitine is the only one
of relevance for dogs with cardiac disease.

correction of a deficiency, improved myocardial metabolic efficiency, and increased antioxidant

protection. Controlled prospective studies will be necessary to accurately judge the efficacy of this

5 - General issues in feeding dogs

with cardiac disease

Dietary modification in dogs needs to be individualized - not all dogs with cardiac disease will
need the same dietary formulation. Patients with cardiac disease vary in terms of their clinical
signs, laboratory parameters, and food preferences and these should all affect diet selection. For
example, more severe sodium restriction would be required for a dog with DCM and CHF than
for a dog with asymptomatic DCM. Dogs with cardiac cachexia require a calorically-dense diet
while an overweight dog should be fed a calorically-restricted diet. Dogs with cardiac disease may
be hyper-, hypo-, or normokalemic and this will influence the choice of diet.

Concurrent diseases also influence diet choice and, in one study, concurrent diseases were present
in 61% of dogs with cardiac disease (Freeman et al, 2003b). For example, a dog with CVD and
colitis would need a diet that is sodium restricted but also one that has nutritional modifications

to help manage the colitis (eg, reduced fat, increased fiber).

Based on these patient parameters, a diet or diets can be selected for the individual patient. There
currently are a number of commercial veterinary diets available that are specifically designed for
animals with cardiac disease. Specific characteristics of these foods vary, but they are moderately
to severely sodium restricted and generally contain increased levels of B vitamins. Some cardiac
diets also may include increased levels of taurine, carnitine, antioxidants, or n-3 fatty acids. In
some cases, a “cardiac” diet may not be needed as some over-the-counter diets may have the pro-
perties desired for an individual dog. The authors also recommend offering more than one diet
that would be appropriate for a dog so that the owner can see which is most palatable to the pet.
Having a number of dietary choices is particularly beneficial for more severely affected CHF
patients, in which a cyclical or selective loss of appetite is common.

In addition to the dog food(s) selected, one must also give the owner careful instructions on treats
and table food. In some cases, dogs may be eating an ideal dog food but are getting large amounts
of sodium from treats. In one study, over 90% of dogs with cardiac disease received treats and these
dogs were receiving up to 100% of their sodium (median, 25%) from treats (Freeman et al, 2003b).

Therefore, in addition to finding a diet that has the desired nutritional properties and palatabili-
ty, it also is important to devise an overall dietary plan that meets the owner's expectations. This

5 - General issues in feeding dogs with cardiac disease

includes devising a satisfactory method for administering medications. Most people administering
medications to their dogs use foods as a way to administer the medication (Freeman et al, 2003b).
Discussing appropriate options for an owner to use for this purpose is necessary, as the foods most
commonly used by owners are very high in sodium (eg, cheese, lunch meats, etc). Including all
forms of dietary intake in the overall diet plan is important to achieve success with nutritional

In many cases, the desired nutrient modifications can be achieved through diet alone. However,
supplementation of certain nutrients may be desirable if they are either not in a particular diet or
not at high enough levels to achieve the desired effect. One issue with the administration of die-
tary supplements is that they should not take the place of standard cardiac medications (eg, ACE
inhibitors, diuretics). Dogs with severe CHF may be receiving 10-20 pills per day and it may be
difficult for the owner to give supplements on top of this without discontinuing one or more of
the cardiac medications. It is important to ask each owner about any dietary supplements being
used as this is often not information that is volunteered (ie, dietary supplements are often not
considered medications or diet). This will help to determine if any
harmful supplements are being given and if the supplements are
being given at an appropriate dose. In situations in which pill admi-
There currently are a number of commercial veterinary diets available nistration is becoming overwhelming for an owner, the veterinarian
that are specifically designed for animals with cardiac disease. Specific can assist the owner in determining which dietary supplements have
characteristics of these foods vary, but they are moderately to severely the least potential benefits and can be discontinued.
sodium restricted and generally contain increased levels of B vitamins.
Some cardiac diets also may include increased levels of taurine, Finally, owners should be aware that dietary supplements are not
carnitine, antioxidants, or n-3 fatty acids.
regulated in the same way as drugs. They do not require proof of safe-
ty, efficacy, or quality control before they can be sold. Therefore,
careful selection of type, dose, and brand is important to avoid toxi-
cities or complete lack of efficacy.


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combined therapy with captopril, furosemide, and a


Home-prepared diets

Example 1

(1000 g diet)

Pork, shoulder with skin . . . . . . . . . . . . . . . . . . 525 g

Rice, cooked . . . . . . . . . . . . . . . . . . . . . . . . . . . 435 g
Wheat bran . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 g
Rapeseed oil . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10 g

Add a low-sodium mineral and vitamin supplement.


The diet prepared in this way contains 30% dry matter Energy value (metabolizable energy) 1810 kcal/1000 g diet
and 70% water prepared (5990 kcal/1000 g DM)

% dry matter g/1000 kcal Dog’s weight (kg)* Daily amount (g)** Dog’s weight (kg)* Daily amount (g)**

Protein 31 59 2 120 45 1250

Fat 28 55 4 200 50 1350

Available carbohydrate 34 66 6 280 55 1450

Fiber 4 9 10 400 60 1550


15 550 65 1640

20 680 70 1740

25 800 75 1830
Key Points 30 920 80 1920
- Energy concentration to combat cardiac 35 1030 85 2010
40 1140 90 2100
- Moderated sodium content to facilitate the
work of the heart

*The diet is offered in accordance with the dog’s healthy weight. For obesity, the diet must be prescribed in accordance with the ideal weight and not
the real weight of the dog.
** Dividing the diet into two meals is recommended to promote proper digestion.

Home-prepared diets
Example 2

(1000 g diet)

Tuna . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 500 g
Rice, cooked . . . . . . . . . . . . . . . . . . . . . . . . . . . 450 g
Wheat bran . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 g
Rapeseed oil . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 g

Add a low-sodium mineral and vitamin supplement.


Energy value (metabolizable energy) 1935 kcal/1000 g diet The diet prepared in this way contains 37% dry matter
prepared (5180 kcal/1000 g DM) and 63% water

Dog’s weight (kg)* Daily amount (g)** Dog’s weight (kg)* Daily amount (g)** % dry matter g/1000 kcal

2 110 45 1170 Protein 33 63

4 190 50 1260 Fat 28 54

6 260 55 1360 Available carbohydrate 33 64

10 380 60 1450 Fiber 4 7

15 510 65 1540

20 640 70 1630

25 750 75 1710
30 860 80 1800

35 970 85 1880 Gestation

40 1070 90 1960 Growth
State of sodium depletion

Examples of home-made diets are proposed by Pr Patrick Nguyen

(Nutrition and Endocrinology Unit; Biology and Pathology Department, National veterinary School of Nantes)

Royal Canin Nutritional Information

© Lanceau
The majority of cardiac dogs suffer from systolic failure due either to acquired chronic valvular disease
(endocardiosis) or dilated cardiomyopathy (DCM). The former disease very often affects small-breed dogs.
DCM is most common in large-breed dogs.

Key Points
to remember:

The role of nutrition

in cardiac disease
• One of the main goals of dietetic • Severe sodium restriction has been • Arginine is a precursor of nitric
strategy is to achieve optimal body inappropriately recommended for oxide (NO), which has been identi-
weight whatever the initial situa- far too long. Its application is fied as a relaxation factor for the
tion: obesity (especially in case of a unwarranted in the initial stages of smooth muscle of blood vessels.
subclinical disease) or cachexia in heart failure, as it risks hastening the Supplementary arginine intake will
some severe cardiac diseases. progression of the cardiac disease by indirectly help combat hypertension.
Anorexia is a common phenomenon activating the renin-angiotensin sys-
in cardiac patients that needs to be tem, especially when angiotensin • L-carnitine is concentrated in the
given due consideration: it is one of converting enzyme (ACE) inhibitors striated muscles and the heart
the main reasons for the request to are simultaneously prescribed. where it plays a key role in providing
euthanize patients with severe car- energy to the cells. L-carnitine defi-

diac disease. It may be directly linked A moderate restriction of sodium ciency has been suggested in connec-
to respiratory problems, to fatigue content (< 80-100 mg/100 kcal) is suf- tion with dilated cardiomyopathy.
accompanying heart failure, to nau- ficient for stages I and II of heart fai- Clinical improvements have been
sea induced by medication or to poor lure. Only severe heart failure justi- reported after the administration of
palatability of certain cardiac diets, fies restricting sodium content to a supplement, although several
containing low sodium and protein 50 mg/100 kcal. months of treatment are necessary
content. to achieve changes that can be
• A cardiac dog must receive a nor- detectable by echocardiography.
Selecting a palatable food, giving mal intake of high quality proteins
frequent small meals and encoura- to combat cardiac cachexia. Limiting • Free radicals, which are responsible
ging the dog to eat are all measures the protein intake is not indicated, for oxidation of membranous phos-
that should not be neglected in except for concomitant hepatic ence- pholipids, aggravate cardiac lesions.
therapeutic management. phalopathy or kidney disease that Oxidative stress is a causal factor of
demands such a restriction. Taurine dilated cardiomyopathy. The daily
• Cardiac dogs often suffer from a supplementation is recommended as administration of antioxidants in
deficiency of EPA-DHA, long-chain n- this sulfated amino acid has positive the food is one of the main ways of
3 fatty acids. A food with a higher properties that can prove effective in combating the progression of heart
EPA-DHA content facilitates the the prevention and treatment of failure.
treatment of cardiac cachexia. dilated cardiomyopathy.

344 344
Royal Canin Nutritional Information

Focus on:


Taurine accounts for at least 40% of 2. It has an antiarrhythmic role (Satoh The correlation has especially been
the pool of free amino acids in the & Sperelakis, 1998). shown in Newfoundland dogs in the
heart. This amino acid is normally United Kingdom (Dukes-McEwan et al,
synthesized in the dog from methio- 3. It helps preserve the integrity of 2001). Positive responses to taurine
nine and cystine. The taurine cardiac muscle cells: in vitro taurine supplementation have been noted in
concentration can be limited in cer- prevents myocyte hypertrophy indu- Boxers suffering from DCM. It is the-
tain conditions such as when the ani- ced by angiotensin II (Takahahsi et al, refore advisable to provide sufficient
mal receives a food with reduced 1998). quantities of taurine in the food to
protein content or when taurine syn- It has long been known that taurine prevent any risk of deficiency.
thesis is insufficient, as is the case in deficiency can provoke degeneration
some breeds and some lines. The syn- of the retina and slow down growth.
thesis of taurine appears to be much Only recently has DCM in dogs been
less efficient in large-breed dogs (> associated with extremely low plas-
35 kg) compared to Beagles (Ko et al, ma taurine levels.

A simple blood sample will help

taurine deficiency. Taurine analysis WITH DILATED CARDIOMYOPATHY
should be performed on whole
blood as taurine is stored predomi-
nantly in blood cells. The plasma
taurine concentration does not pro-
perly reflect the muscular and car-
diac storage of taurine.

Taurine is essential to the contracti-

lity of the heart muscle.

1. It has a positive or negative

© Bussadori

inotropic effect depending on whe-

ther calcium is abundant or not in
the cells; taurine protects the myo- Generalized cardiomegaly during cardiomyopathy
cytes against the effects of excess with clinical signs.
calcium (Satoh & Sperelakis, 1998).

Dukes-McEwan J, Biourge V, Ridyard A et al Ko K, Backus RC, Berg JR et al - In vivo tau- Takahahsi K, Azuma M, Baba A et al -
- Dilated cardiomyopathy in Newfoundland rine biosynthesis is greater in small dogs than Taurine improves angiotensin II-induced hyper-
dogs: association with low whole blood taurine large dogs. Waltham International Nutritional trophy of cultured neonatal rat heart cells. Adv
level. Proceedings of the British Small Animal Sciences Symposium, Sept 15, 2005; Exp Med Biol 1998; 442: 129-135.
Veterinary Association Congress J Small Anim Washington DC, USA.
Pract 2001: 500.
Satoh H, Sperelakis N - Review of some
actions of taurine on ion channels of cardiac
muscle cells and others. Gen Pharmacol 1998;
30(4): 451-63.

345 345
Royal Canin Nutritional Information

Summary of select publications…

There is a hypothesis associating dila- to evaluate the taurine status of a nical and echocardiography exami-
ted cardiomyopathy (DCM) in dogs, group of Newfoundland dogs in the nations. The evaluation of taurine
especially large breeds, with taurine United Kingdom. One hundred and status was based on total blood ana-
deficiency. This study was designed four Newfoundlands underwent cli- lysis (nmol/mL). In addition, a detai-
led dietary history was obtained for
each dog. The echocardiography
examinations permited the classifica-
tion of dogs as normal, dogs with
dilated cardiomyopathy, dogs with a
reduction in shortening fraction or
dogs presenting with dilatation of
the left ventricle.

A low taurine concentration is consi-

dered less than 200 nmol/mL, and a
very low taurine level is less than
130 nmol/mL.
© Psaila


Total blood taurine concentration

Average < 200 nmol/mL <130 nmol/mL


Normal dogs (n=49) 247±73 7 3

Dog with a reduction

215±67 14 4
in the shortening fraction (n=39)

Dogs with DCM (n=11) 184±62 3 4

Dogs with dilatation

187±116 3 1
of the left ventricle (n=5)

The taurine concentrations are significantly lower in dogs with DCM compared with normal dogs (ANOVA p=0.02)


Biourge V, Dukes-McEwan J, Desprez G et al -

Association between low whole blood taurine
and Dilated CardioMyopathy (DCM) In
Newfoundland dogs. ESVCN 2001, abstract.

346 346
Royal Canin Nutritional Information

A low taurine concentration has

been shown in a significant number
of Newfoundland dogs. In this study
population, the taurine values ten-
ded to be lower than in dogs with
dilated cardiomyopathy (DCM). The
purpose of this study was to test the
impact of taurine or methionine sup-
plementation in correcting taurine

Forty-eight dogs with a blood taurine

value less than 200 nmol/mL were
identified. Echocardiography exami-
nation enabled the establishment of
three categories of dogs: normal,
echocardiography anomalies without
clinical signs (e.g. reduced contractili-
ty or dilatation of the left ventricle)
and dogs with clinical DCM.

The dogs with clinical DCM received

© Lenfant
1000 mg of taurine by mouth twice a
day. The remaining dogs were mat-
ched by age and sex and then recei-
ved 250 mg of taurine or 750 mg of study to 324±14 nmol/mL after three These results suggest that 250 mg of
methionine per os twice a day. Four months of supplementation and taurine or 750 mg of methionine per
dogs were fed with a specific food 275±10 nmol/mL after six months of os twice a day, and a diet providing
for very-large dogs. supplementation. No differences 1000 mg of taurine/kg normalizes
could be distinguished with respect the taurine concentration in taurine
The blood and urine taurine concen- to the type or dose of supplementa- deficient Newfoundland dogs. For
tration, as well as the urine creatini- tion. the dogs in this study, a low taurine
ne concentration were measured status cannot be explained by grea-
after three and six months of supple- The urine taurine/creatinine ratio ter taurine losses or an inability to
mentation and compared with the was minimal at the start of the study, utilize methionine as a taurine pre-
initial values. increasing significantly with supple- cursor.

mentation of methionine or taurine,
The blood taurine concentration more makedly with the highest taurine
increased in all the dogs. It rose from concentration.
144±8 nmol/mL at the start of the


Willitz R, Desprez G, Duke-McEwans J et al -

Six months taurine or methionine supplementa-
tion in 53 Newfoundland Dogs suffering from
low whole blood taurine. ESCVN 2002,

347 347